Comorbid physical conditions may be more common in people with autism spectrum disorder (ASD) than other people.

To identify what is and what is not known about comorbid physical conditions in people with ASD.

We undertook an umbrella systematic review of systematic reviews and meta-analyses on comorbid physical conditions in people with ASD. Five databases were searched. There were strict inclusion/exclusion criteria. We undertook double reviewing for eligibility, systematic data extraction and quality assessment. Prospective PROSPERO registration: CRD42015020896.

In total, 24 of 5552 retrieved articles were included, 15 on children, 1 on adults, and 8 both on children and adults. Although the quality of included reviews was good, most reported several limitations in the studies they included and considerable heterogeneity. Comorbid physical conditions are common, and some are more prevalent than in the general population: sleep problems, epilepsy, sensory impairments, atopy, autoimmune disorders and obesity. Asthma is not. However, there are substantial gaps in the evidence base. Fewer studies have been undertaken on other conditions and some findings are inconsistent.

Comorbid physical conditions occur more commonly in people with ASD, but the evidence base is slim and more research is needed. Some comorbidities compound care if clinicians are unaware, for example sensory impairments, given the communication needs of people with ASD. Others, such as obesity, can lead to an array of other conditions, disadvantages and early mortality. It is essential that potentially modifiable physical conditions are identified to ensure people with ASD achieve their best outcomes. Heightening clinicians’ awareness is important to aid in assessments and differential diagnoses, and to improve healthcare.

Children with autism spectrum disorder (ASD) have increased susceptibility to anxiety disorders. Variation in a common ASD symptom, insistence on sameness behaviour, may predict future anxiety symptoms.

To describe the joint heterogeneous longitudinal trajectories of insistence on sameness and anxiety in children with ASD and to characterise subgroups at higher risk for anxiety.

In a longitudinal ASD cohort (n = 421), insistence on sameness behaviour was measured using the Autism Diagnostic Interview-Revised at approximately ages 3, 6 and 11 years. Anxiety was quantified at 8 time points between ages 3 and 11 years using the Child Behavior Checklist (CBCL) (parent report). Clusters of participants following similar trajectories were identified using group-based and joint trajectory modelling.

Three insistence on sameness trajectories were identified: (a) ‘low-stable’ (41.7% of participants), (b) ‘moderate-increasing’ (52.0%) and (c) ‘high-peaking’ (i.e. increasing then stabilising/decreasing behaviour) (6.3%). Four anxiety trajectories were identified: (a) ‘low-increasing’ (51.0%), (b) ‘moderate-decreasing’ (16.2%), (c) ‘moderate-increasing’ (19.6%) and (d) ‘high-stable’ (13.1%). Of those assigned to the ‘high-peaking’ insistence on sameness trajectory, 95% jointly followed an anxiety trajectory that surpassed the threshold for clinical concern (T-score >65) by middle childhood (anxiety trajectories 3 or 4). Insistence on sameness and anxiety trajectories were similar in severity and direction for 64% of the sample; for 36%, incongruous patterns were seen (e.g. decreasing anxiety and increasing insistence on sameness).

The concurrent assessment of insistence on sameness behaviour and anxiety in ASD may help in understanding current symptom profiles and anticipating future trajectories. High preschool insistence on sameness in particular may be associated with elevated current or future anxiety symptoms.

Research on women with the fragile-X premutation (FX-p) has been underrepresented within the field of behavioural phenotypes.

To understand whether the FX-p confers risk for autistic traits, depression and anxiety, independent of maternal status.

In study 1, mothers of children with fragile-X syndrome (M-FXp; n = 51, mean age 43 years (s.d. = 5.80)) were compared with mothers of autistic children (M-ASD; n = 59, mean age 42 (s.d. = 5.80)), mothers of children with Smith-Magenis syndrome (M-SMS; n = 27, mean age 39 (s.d. = 7.20)) and mothers of typically developing children (M-TD; n = 44, mean age 40 (s.d. = 4.90)). In study 2, the M-FXp group were compared with non-mothers with the FX-p (NM-FXp; n = 17, mean age 32 (s.d. = 9.20)), typically developed non-mothers (NM-TD; n = 28, mean age 31 (s.d. = 6.80)) and the M-TD group. All participants completed an online survey, including measures of IQ, autistic traits, anxiety, depression and positive affect.

In study 1: the M-FXp group reported more autistic traits than the M-TD group (P < 0.05, η2 = 0.046). Anxiety and parental stress were elevated in the M-FXp, M-SMS and M-ASD groups relative to the M-TD group (all P ≤ 0.003, η2 = 0.079–0.322). In study 2: a main effect of premutation status indicated that women with the FX-p report elevated autistic traits and anxiety (P ≤ 0.007, η2 = 0.055–0.060); this did not interact with maternal status.

The findings indicate that women with the FX-p show an increased risk for autistic traits and anxiety. This risk is specific to the presence of the FX-p and is not fully accounted for by maternal status or the stress of caring for children with neurodevelopmental disorders.

Although attention-deficit hyperactivity disorder (ADHD) is classified as a neurodevelopmental disorder in the latest diagnostic manuals, it shows phenotypic and genetic associations of similar magnitudes across neurodevelopmental, externalising and internalising disorders.

To investigate if ADHD is aetiologically more closely related to neurodevelopmental than externalising or internalising disorder clusters, after accounting for a general psychopathology factor.

Full and maternal half-sibling pairs (N = 774 416), born between 1980 and 1995, were identified from the Swedish Medical Birth and Multi-Generation Registers, and ICD diagnoses were obtained from the Swedish National Patient Register. A higher-order confirmatory factor analytic model was fitted to examine associations between ADHD and a general psychopathology factor, as well as a neurodevelopmental, externalising and internalising subfactor. Quantitative genetic modelling was performed to estimate the extent to which genetic, shared and non-shared environmental effects influenced the associations with ADHD.

ADHD was significantly and strongly associated with all three factors (r = 0.67–0.75). However, after controlling for a general psychopathology factor, only the association between ADHD and the neurodevelopmental-specific factor remained moderately strong (r = 0.43, 95% CI = 0.42–0.45) and was almost entirely influenced by genetic effects. In contrast, the association between ADHD and the externalising-specific factor was smaller (r = 0.25, 95% CI = 0.24–0.27), and largely influenced by non-shared environmental effects. There remained no internalising-specific factor after accounting for a general factor.

Findings suggest that ADHD comorbidity is largely explained by genetically influenced general psychopathology, but the strong link between ADHD and other neurodevelopmental disorders is also substantially driven by unique genetic influences.

Population studies have suggested that most adults with attention-deficit hyperactivity disorder (ADHD) did not have the disorder in childhood, challenging the neurodevelopmental conceptualisation of ADHD. Arbitrary definitions of age at onset and lack of defined trajectories were accounted for the findings.

The objective of this study was to assess the proportion of individuals presenting with either a neurodevelopmental trajectory or late-onset disorder, and to assess risk factors associated with them.

Data of 4676 individuals from the 1993 Pelotas birth cohort at 11, 15, 18 and 22 years of age were used. Polythetic and latent class mixed model analyses were performed to define ADHD trajectories from childhood to adulthood, and characterise the neurodevelopmental or late-onset courses. Regression models were applied to assess factors associated with different trajectories.

Classical polythetic analyses showed that 67% of those with ADHD at 22 years of age had a neurodevelopmental course of the disorder. Latent class mixed model analysis indicated that 78% of adults with ADHD had a trajectory of persistent symptoms, more common in males. The remaining adults with ADHD had an ascending symptom trajectory that occurred after puberty, with late-onset ADHD associated with female gender and higher IQ.

Both polythetic and latent trajectories analyses provided empirical evidence supporting that the large majority of adults with ADHD had a neurodevelopmental disorder.

Intellectual and developmental disabilities (IDDs) and psychiatric disorders frequently co-occur. Although each has been associated with negative outcomes, their combined effect has rarely been studied.

To examine the likelihood of five negative health and healthcare outcomes for adults with IDD and mental health/addiction disorders (MHAs), both separately and together. For each outcome, demographic, clinical and system-level factors were also examined.

Linked administrative data-sets were used to identify adults in Ontario, Canada, with IDD and MHA (n = 29 476), IDD-only (n = 35 223) and MHA-only (n = 727 591). Five outcomes (30-day readmission, 30-day repeat ED visit, delayed discharge, long-term care admission and premature mortality) were examined by logistic regression models with generalised estimating equation or survival analyses. For each outcome, crude (disorder groups only) and complete (adding biosocial covariates) models were run using a general population reference group.

The IDD and MHA group had the highest proportions across outcomes for both crude and complete models. They had the highest adjusted ratios for readmissions (aOR 1.93, 95%CI 1.88–1.99), repeat ED visit (aOR 2.00, 95%CI 1.98–2.02) and long-term care admission (aHR 12.19, 95%CI 10.84–13.71). For delayed discharge, the IDD and MHA and IDD-only groups had similar results (aOR 2.00 (95%CI 1.90–2.11) and 2.21 (95%CI 2.07–2.36). For premature mortality, the adjusted ratios were similar for all groups.

Poorer outcomes for adults with IDD, particularly those with MHA, suggest a need for a comprehensive, system-wide approach spanning health, disability and social support.

Psychotropics are overprescribed for adults with intellectual disabilities; there are few studies in children and young people.

To investigate antipsychotic and antidepressant prescribing in children and young people with and without intellectual disabilities, and prescribing trends.

Scotland's annual Pupil Census, which identifies pupils with and without intellectual disabilities, was record-linked to the Prescribing Information System. Antidepressant and antipsychotic data were extracted. Logistic regression was used to analyse prescribing between 2010 and 2013.

Of the 704 297 pupils, 16 142 (2.29%) had a record of intellectual disabilities. Antipsychotic and antidepressant use increased over time, and was higher in older pupils; antipsychotic use was higher in boys, and antidepressant use was higher in girls. Overall, antipsychotics were prescribed to 281 (1.74%) pupils with intellectual disabilities and 802 (0.12%) without (adjusted odds ratio 16.85, 95% CI 15.29–18.56). The higher use among those with intellectual disabilities fell each year (adjusted odds ratio 20.19 in 2010 v. 14.24 in 2013). Overall, 191 (1.18%) pupils with intellectual disabilities and 4561 (0.66%) without were prescribed antidepressants (adjusted odds ratio 2.28, 95% CI 2.03–2.56). The difference decreased each year (adjusted odds ratio 3.10 in 2010 v. 2.02 in 2013).

Significantly more pupils with intellectual disabilities are prescribed antipsychotics and antidepressants than are other pupils. Prescribing overall increased over time, but less so for pupils with intellectual disabilities; either they are not receiving the same treatment advances as other pupils, or possible overprescribing in the past is changing. More longitudinal data are required.